Centrosomes, which consist of a centriole pair and pericentriolar material (PCM), are the primary microtubule-organizing centers (MTOCs) in most cells. In Caenorhabditis elegans, the kinase ZYG-1 is essential for the replication of centrosomes. Embryos lacking maternal ZYG-1 activity fail to replicate the paternally contributed centriole pair, and are thus unable to form bipolar spindles following first division. In contrast, loss of paternal ZYG-1 activity results in duplication failure during male meiosis, and the production of sperm with a single centriole. These sperm can still fertilize eggs but the resulting embryos assemble a monopolar rather than bipolar spindle at first division. Several recently published reports indicated that centrosome duplication might be regulated differently in different tissues. To investigate this in C. elegans, we have been analyzing the effect of zyg-1 mutations on the male and female germ lines. We have found that small truncations of the c-terminus of ZYG-1 cause a novel phenotype: the production of embryos with supernumerary replication-incompetent centrosomes. These embryos inherit up to eight centrioles that are unable to duplicate. We have found the extra centrioles arise solely from defects in the male germ line and that this phenotype behaves as a gain of function. In contrast, failure of mutant embryos to duplicate these centrosomes is due to a loss of function of maternal ZYG-1. Thus, a single mutation behaves as a loss-of-function allele in one developmental context and a gain-of-function allele in another, suggesting that ZYG-1 is subject to different forms of regulation in different tissues. Consistent with this, we find that these mutant forms of ZYG-1 localize normally to meiotic centrosomes but are almost absent from mitotic centrosomes. To investigate this further, we characterized centrosome behavior during meiosis in live and fixed spermatocytes. We find that centrosomes behave normally through the end of meiosis I but rapidly amplify as cells approach meiosis II. Amplification of centrosomes depends upon the centrosome duplication factor SAS-6, consistent with an overreplication defect. We are currently investigating the possibility that cyclin dependent kinase 1 (cdk-1), an inhibitor of centrosome duplication, might interact with ZYG-1 to regulate centrosome duplication during meiosis and mitosis.